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Although certain arrhythmias are more common in neonates and
young infants compared to older children and adults, all types of
arrhythmias can occur. Many are benign and do not cause hemodynamic
compromise. Others may compromise cardiac output and cause decreased
blood pressure and decreased perfusion. Sustained tachyarrhythmias
may eventually cause myocardial dysfunction, which is known as tachycardia-induced
cardiomyopathy. The purpose of this chapter is to review diagnosis
and management of common arrhythmias in neonates and young infants.

Normally the electrical impulse originates in the sinoatrial
(SA) node. The atrioventricular (AV) node, His bundle, and bundle
branches provide the only normal pathway for transmission of impulses
between the atria and ventricles. Generation of impulses from the
SA node is modulated by many factors including body temperature,
blood pressure, autonomic nervous system, and circulating catecholamines.
Conduction through the AV node is slowed so that atrial contraction
is complete before ventricular contraction occurs.

Abnormal Impulse Formation

Abnormalities in impulse formation result in sinus bradycardia
and tachycardia, premature atrial and ventricular contractions,
and ectopic or automatic rhythms from the atria, AV node, or ventricles.
Automatic tachycardias are usually incessant meaning that they are
almost always present. Increased automaticity occurs when atrial,
nodal, or ventricular cells display autonomous repetitive depolarization
at a higher rate than is normal. Sinus tachycardia, atrial ectopic
tachycardia, junctional ectopic tachycardia, and the automatic form
of ventricular tachycardia are all forms of automatic tachycardia.
Onset and termination are often gradual rather than abrupt. The
rate of automatic tachycardias is often sensitive to changes in
autonomic tone. Therapies that produce only transient effects, for
example, direct current (DC) cardioversion and administration of
adenosine, do not terminate automatic tachycardias.

Abnormal Impulse Conduction

Reentry, the other form of abnormal impulse conduction, is an
important mechanism underlying supraventricular tachycardia (SVT)
in infants. The reentrant circuit involves two functionally distinct
pathways that have different conduction velocities and refractory
periods. Unidirectional block is present in one pathway, an electrical
impulse traverses the other pathway and conduction is delayed enough
so that the impulse is able to “reenter” the blocked
pathway from the other direction thus completing the reentrant circuit.
Reentry mechanisms usually cause paroxysmal tachycardias, which
may start and stop multiple times in the course of the day. Reentrant
tachycardias start and stop abruptly and they often terminate in
response to interventions that produce only transient effects (eg,
adenosine) because interruption of the reentrant circuit usually
terminates the tachycardia.

Sinus arrhythmia is a normal phasic variation in impulse formation
from the SA node that is often in cycle with respiration (Figure
10-1). This is the most common cause of an irregular heart rate, especially
in older infants. The P-wave ...